SLEEP AND CIRCADIAN RHYTHMS IN RELATION TO ANDROGEN STATUS IN MIDDLE-AGED MEN: CURRENT EVIDENCE AND CLINICAL IMPLICATIONS

Testosterone secretion in men exhibits pronounced temporal variation and is closely associated with the sleep–wake cycle. Short sleep duration, sleep fragmentation, obstructive sleep apnea, night-shift work, and circadian misalignment are common in modern populations and may interact with age, obesity, and etabolic dysfunction in shaping androgen status. To summarize current evidence on the associations of sleep duration, sleep architecture, circadian rhythms, shift work, and sleep-disordered breathing with circulating testosterone concentrations in men, with particular attention to middle age. A narrative review of relevant clinical, experimental, and epidemiological studies, systematic reviews, and meta-analyses was conducted. PubMed/MEDLINE-indexed publications were prioritized. Search concepts included combinations of the terms testosterone, androgen status, sleep duration, sleep deprivation, sleep quality, slowwave sleep, circadian rhythm, shift work, obstructive sleep apnea, and men. Human studies with laboratory assessment of testosterone were given priority. Testosterone concentrations increase after sleep onset and generally reach higher levels during nocturnal sleep and in the early morning. Evidence regarding partial sleep restriction is heterogeneous. A metaanalysis of 18 studies involving 252 men found no statistically significant reduction in testosterone after short-term partial sleep deprivation, whereas total sleep deprivation of 24 hours or longer significantly reduced testosterone concentrations. Selective suppression of slow-wave sleep has also been associated with lower morning testosterone levels. Obstructive sleep apnea is consistently associated with lower testosterone levels in meta-analyses, especially in severe disease, although obesity and metabolic dysfunction contribute substantially to this relationship. Evidence regarding night-shift work remains inconsistent. Experimental data also suggest that molecular clock components, including CLOCK, BMAL1, PER, and CRY, may participate in the regulation of Leydig-cell steroidogenesis. Sleep and circadian organization are biologically relevant to androgen homeostasis in men. However, current evidence does not support a simple causal model in which every reduction in sleep duration inevitably causes testosterone deficiency. Sleep architecture, obstructive sleep apnea, obesity, metabolic status, work schedule, and the timing of testosterone measurement should be considered jointly when evaluating androgen status in middle-aged men.